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目的通过观察表没食子儿茶素没食子酸酯(EGCG)对刀豆蛋白A(ConA)诱导的肝损伤小鼠Bcl-2、Bax蛋白表达的影响探讨EGCG对肝脏的保护机制。方法将C57BL/6小鼠随机分为对照组、EGCG组、ConA模型组、EGCG+ConA组4组。通过静脉注射ConA建造急性肝损伤模型,并予EGCG进行干预,采用免疫组化技术及Western-blot检测各组小鼠肝组织中Bcl-2、Bax的表达。结果 ConA模型组小鼠肝组织Bax的表达明显增加,与对照组比较差异有统计学意义(P<0.05);给予EGCG治疗后Bax表达下降,与ConA模型组比较,差异有统计学意义(P<0.05)。ConA模型组小鼠肝组织Bcl-2的表达减少,与对照组比较差异有统计学意义(P<0.05);EGCG+ConA组Bcl-2的表达增多,与ConA模型组比较差异有统计学意义(P<0.05)。结论 EGCG对免疫性肝损伤有保护作用,其机制可能与调节Bcl-2及Bax的表达有关。
Objective To observe the effect of epigallocatechin-3-gallate (EGCG) on the expression of Bcl-2 and Bax in ConA-induced liver injury mice and to explore the protective mechanism of EGCG on liver. Methods C57BL / 6 mice were randomly divided into control group, EGCG group, ConA model group and EGCG + ConA group. The model of acute liver injury was established by intravenous injection of ConA. The model was induced by EGCG. The expression of Bcl-2 and Bax in liver tissue of each group was detected by immunohistochemistry and Western-blot. Results The expression of Bax in liver tissue of ConA model group was significantly increased compared with that of control group (P <0.05), while the expression of Bax was decreased after EGCG treatment. Compared with ConA model group, the difference was statistically significant (P <0.05). Compared with control group, the expression of Bcl-2 in ConA model group decreased significantly (P <0.05); the expression of Bcl-2 in EGCG + ConA group increased significantly compared with ConA model group (P <0.05). Conclusion EGCG has a protective effect on autoimmune liver injury, and its mechanism may be related to the regulation of Bcl-2 and Bax expression.